Decoding-based reading disorder (RD; or dyslexia) is a highly prevalent neurodevelopmental disorder that often persists into adulthood. Poor literacy in adulthood has negative impact on socioeconomic and educational outcomes, which in turn affect the outcomes of subsequent generations. Despite significant consequences, research on RD adults is severely lagging. There is also increasing interest in understanding compensatory mechanisms in RD, which are thought to develop into adulthood. Compensation in RD allows for less efficient but functional reading abilities, and is thought to be supported by alternative linguistic, cognitive and sensory processing strategies and their underlying neural pathways. This is in contrast to the more typical `reading network' found in the left posterior brain system. Neurocognitive mechanisms of compensation are however, far from understood. This in part because the operational definitions of compensation have been ambiguous, and because functional MRI approaches most often used in compensation research are inherently correlational in nature. For example, it is currently unknown whether the proposed compensatory processes are causally related to reading behaviors in compensated RD or whether they are epiphenomena. The degree to which various alternative neural pathways are recruited and contribute to individual differences in compensatory abilities is also unknown. This proposal addresses these scientific gaps by building on our past work on the neurocognitive mechanisms of adult RD and compensation using an experimental neuromodulation technique, transcranial magnetic stimulation (TMS), coupled with multimodal neuroimaging including MR Spectroscopy (MRS) of gamma-aminobutyric acid (GABA) and glutamate, and functional MRI. In this proposal, (1) We will identify neurocognitive profiles of compensated RD adults compared to persistent RD adults with continued reading difficulties as well as typical readers with no RD history. We also identify neurocognitive mechanisms and networks underlying individual differences in current reading ability (regardless of past RD diagnosis) and past RD diagnosis (regardless of current reading ability). (2) Using transcranial magnetic stimulation (TMS) within an experimental, hypothesis testing paradigm, we will discover the processes underlying short-term functional reorganization and its impact on reading in key neural nodes thought to be critical for reading, RD and compensation. Through TMS-induced neuromodulation, we systematically test hypotheses regarding causal processes thought to be involved in compensation. (3) In order to address hypotheses regarding the neurochemical mechanisms underlying compensatory processes and pathways, we will discover how regionally specific levels of GABA, important for modulation of cortical excitability, predict responses to TMS-induced (meta)plasticity. Such work will not only advance theories of RD and compensation, but ultimately may improve strategies to promote intervention models and successful compensation in RD, in both children and adults with RD.